Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharm II > Lecture 2 (Cardio)-Exam1 > Flashcards

Lecture 2 (Cardio)-Exam1 Flashcards

1
Q

What does Aldosterone do normal and when blocked?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is steps one, two, and three of primary homeostasis?

A

(1) Vasoconstriction – endothelin
* Reflexive contraction of vessel
* Decreased blood flow (dec. bleeding)

(2) Exposure – exposed collagen from damaged endothelium releases vWF
* vWF binds to the exposed collagen

(3) Adhersion-platelets bind to vWF via glycoprotein 1B (GP1B)
* After vWF is bound to collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is step 4 of primary hemostasis?

A

Activation – active platelets change shape (release chemicals)
* Release more vWF, serotonin, ADP, and thromboxane A2, Ca (important for clotting)
* ADP and thromboxane A2
* Activate more platelets
* Stimulate expression of glycoprotein IIB/IIIA on platelet membrane surface

ADP = adenosine diphosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is step five of primary hemostasis?

A

Aggregation – GPIIB/IIIA links platelets together via fibrinogen and form a platelet plug

Platelet plug to move to secondary hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Fill in for antiplatelet drugs

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Antiplatelet therapy: Aspirin
* What is the MOA of aspirin?
* What type of drug is it?

A
  • Activated platelets release arachidonic acid
  • AA is onverted to prostaglandins via COX1 -> prostaglandins releases thromboxane A2
  • Thromboxane A2 promotes activation of more platelets and activation of glycoprotein 2b/3a
  • Aspirin is an irreversible COX inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Antiplatelet therapy: Aspirin
* Blocks what for and for how long?
* First line for what?

A
  • Blocks thromboxane platelet activation for the life of the platelet (7-10 days)
  • First-line prophylactic antiplatelet therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Antiplatelet therapy: ADP receptor inhibitors (P2Y12 inhibitors)
* What are the examples?
* Second line for what?
* What can it be combined with?

A
  • Clopidogrel, ticagrelor, ticlopidine, prasugrel
  • Second-line prophylactic antiplatelet therapy
  • Combined with aspirin for dual antiplatelet therapy (DAPT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the MOA of ADP receptor inhibitors (P2Y12 inhibitors)?

A
  • Bind to the P2Y12 ADP receptor and prevent ADP from binding
  • No ADP binding = no formation of glycoprotein 2b/3a receptors on the surfaced of activated platelets
  • No platelet aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Antiplatelet therapy: Glycoproteint 2b/3a inhibitors
* What are the examples?
* Higest risk of what?
* Only available how?
* Use has what?
* How long do you use it?
* Always given with what?

A
  • Abciximab, eptifibatide, tirofiban
  • Highest risk of bleeding and thrombocytopenia
  • Only available IV
  • Use has declined with the use of DAPT
  • < 24-hour duration
  • Always given with heparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Antiplatelet therapy: Glycoproteint 2b/3a inhibitors
* What is the MOA?
* What is the medication reserved for?

A

MOA:
* Prevent platelet cross linking and aggregation

Reserved for use with interventional cardiac procedures in high-risk patients
* NSTEMI with high cTn
* STEMI not preloaded with a P2Y12 inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Antiplatelet Therapy:
* What are the indications?
* What are the CI?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bleeding with antiplatelet agents:
* What are the sxs of bleeding (low or dysfunctional platelets)?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Bleeding with antiplatelet:
* Serious bleeding rare – MC when?
* CI when?

A
  • Serious bleeding rare – MC when combined with other anticoagulants
  • CI: any active bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Antiplatelet: Aspirin
* What is the MOA?
* What are the SE?
* CI if what?

A
  • Irreversible COX-1 inhibitor
  • SE: GI bleeding and Dyspepsia
  • CI only if true allergy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clopidogrel
* What is the MOA?
* What are the SE?

A

MOA:
* Irreversible P2Y12 receptor blocker
* Prodrug – requires activation in liver by CYP450 enzymes; mostly CYP2C19

SE:
* Dizziness
* Headache
* Palpitations
* GI distress
* Thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Clopidogrel
* Avoid use with what?
* Poor efficacy with what?

A
  • Avoid use with CYP2C19 inhibitors – decrease concentration of active metabolites (decreased efficacy)
  • Poor efficacy with low CYP2C19 metabolizers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Prasugrel
* What is the MOA?
* What are the SE?
* Similar to what?

A
  • Irreversible P2Y12 receptor blocker-> Prodrug – requires activation in liver by CYP2C19
  • SE: Same as Clopidogrel (Dizziness, Headache, Palpitations, GI distress, Thrombocytopenia)
  • Equal efficacy to clopidogrel with more bleeding risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ticagrelor
* What is the MOA?
* What are the SE?

A

MOA:
* Reversible P2Y12 receptor blocker
* Not a prodrug
* Metabolized by CYP3A4

SE:
* Dyspnea
* Nausea
* Dizziness
* Hyperuricemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Cangrelor:
* What is the MOA?
* Only what?

A
  • Reversible P2Y12 receptor blocker
  • Only IV P2Y12 inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Wha tis stable angina? What unstable angina?

A
  • Stable Angina: Myocardial ischemia secondary to exertion (imbalance between myocardial oxygen demand and delivery)
  • Unstable Angina: New, worsening symptoms with activity and/or at rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is NSTEMI and STEMI?

A
  • NSTEMI/NSTE-ACS: Myocardial infarction without ST elevation
  • STEMI/STE-ACS: Myocardial infarction with ST elevation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Stable Angina:
* MC with what?
* What is the most common cause?
* When does pain happen?
* how is the pain?
* Symptoms include what?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Stable angina:
* What is the one txt approach of risk factor modification?

A
  • Slow progression of atherosclerosis and prevent complications
  • Minimum effect on symptom control or QOL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
For stable angina risk factor modification txt, fill in (focus on Lipid and BP management)
26
For stable angina risk factor modification txt, fill in
27
Ace inhibitors/ARBS * Decreases what? * Who is this recommended to?
* Decrease the incidence of cardiovascular death and time to myocardial infarction or stroke in patients with ASCVD * Class I recommendation by the AHA / ACC for all patients with SIHD and HTN, DM, CKD, HFrEF
28
Ace inhibitors/ARBS * What are all the benefits?
29
What is the first line antiplatelet therapy for stable angina ? * What does it block? * What is the dose? Why? * Decreases what?
30
What is the second line antiplatelet therapy for stable angina ?
Second-line: clopidogrel * Aspirin intolerant or contraindicated
31
Stable angina/ stable ischemic heart disease * How do you manage angina?
Decrease ischemic episodes and increase the amount of exercise / exertion prior to chest pain * Minimal survival benefit * Improves symptoms and QOL
32
Management of stable angina-Acute sx with NITRATES * What is the MOA? * What predominates? What does that cause? * Decreases what? * What does it increase? * What else does it dilate and what is the cause?
33
Nitroglycerin * What is the Route? * What is the onset? * What are the indication? * What are the SE?
## Footnote *Headaches usually resolve in 2 to 3 weeks with chronic use and are generally responsive to acetaminophen **Concomitant beta blocker administration may preven
34
What is CI with Nitrates?
CI: Right-sided infarct – hypotension and concomitant use with drugs for ED
35
Acute symptomact treatment: (stable ang) * What is first line? * What can the first line be used for? * What is the Primary effect and secondary effects?
36
Nitroglycerin: * What is the MC route? * What is the dose?
37
Nitroglycerin-patient education * What do you need to say about storage? (3) * Refill when if open? * What does the patient do before taking it? * Keep it where when you take it? * Take when? * Call 911 when?
38
Management of stable angina-prevention: * What is first line? * What is the MOA? * All of them are what? * What is not as effective? * Not indicated for what disease?
39
Management of stable angina-prevention: * What is second line? Why would a patient take this? * Decrease what? * What is the MOA? * What are the examples?
40
41
Fill this in for the prevention of stable angina
Considered 3rd line-long acting nitrates * Need a nitro free period therefore your body does not get use to it
42
Nitroglycerin tolerance: * Can occur when? * What does it impair? * How do you prevent it? How do you do that? What is the issue?
42
Stable angina-revascularization: * PCI or CABG may be indicated in some patients with stable angina. What happened with sxs, mortality and symtom control?
* Persistent symptoms despite maximum medication and lifestyle changes * Does not improve mortality in this population * May provide symptom control ## Footnote AL-Lamee et al Lancet 2018 * 200 patients randomized to PCI or sham procedure * No difference in angina episode frequency, QOL scores or exercise treadmill time between groups
43
Vasospastic angina * What is it? * Less what? * What is it caused why? * What type of ischemia? * Patients generally are what? * What is it assoicated with?
44
Vasospatic angina * What is the treatment?
* Acute attacks – SL nitroglycerin * Chronic suppression – calcium channel blockers * Avoid beta-blockers
45
Acute coronary syndromes (ACS) encompasses what?
ACS encompasses Unstable angina, NSTEMI, and STEMI * NSTE-ACS: NSTEMI and Unstable Angina * STE-ACS: STEMI
46
acute coronary syndrome: * What are changed that suggest change from stable angina to ACS?
* Sudden onset of new angina * Angina at rest * Increased severity of stable angina (> 20 minutes) * Atypical symptoms – SOB, fatigue, dizziness
47
What do you need to order and give with the clinical suspicion of ACS?
48
# Sorry, I know it is a lot for one card but it was more simple things lol Initial assessment-All ACS Patients * Assess what? * What do you need get a preliminary of? * What dx test? * What nees to be attached to patient? * Give what in needed? * What needs to be obtained? * What needs to be brought to bedside? * Rule out what?
49
Initial supportive care: all ACS * What do you need to give? (4)
* Aspirin given – 325 mg chew and swallow x 1 dose * Nitroglycerin given – 0.4 mg up to 3 doses if no contraindications * Morphine – reserved for severe chest pain not relieved by nitroglycerin – not routine (only if cont. CP) * Retrospective studies showed increased risk of death * Mechanism unknown * Beta-blocker within first 24 hours
50
What are the contraindications of nitroglycerin?
51
Unstable * What is it caused by? * What happens to vessle? * What are the ECGs changes? * What is the risk straify (2)
* Ruptured atherosclerotic plaque * Usually ≥ 90% vessel occlusion * ± ECG changes: ST depression or T wave inversions * Risk stratify (TIMI, GRACE, HEART scores) * Low-risk – ischemia driven approach * Intermediate to high risk – early invasive approach | SAME AS NSTEMI
52
NSTEMI * What is it caused by? * What happens to vessle? * What are the ECGs changes? * What is the risk straify (2)
* Ruptured atherosclerotic plaque * Usually ≥ 90% vessel occlusion * ± ECG changes: ST depression or T wave inversions * Risk stratify (TIMI, GRACE, HEART scores) * Low-risk – ischemia driven approach * Intermediate to high risk – early invasive approach | SAME AS UNSTABLE ANGINA
53
What makes Unstable angina and NSTEMI different?
* Unstable: negative troponin (ischemia only) * NSTEMI: Positiv troponin (infarction)
54
NSTEMI: Low risk patients * What is the management? (general)
Medical management – PCI not planned
55
NSTEMI: Low risk patients * What type of therapy early? * What are some other medications does the patient need to be on?
* Early anticoagulation and antithrombotic therapy * Start P2Y12 inhibitor – clopidogrel or ticagrelor (they got aspirin already) * Initiate anticoagulation – enoxaparin or unfractionated heparin (doses vary) * Short-term, discontinued within a few days (unlike DVT)
56
NSTEMI: Low risk patients * What happens if stress test positive? * The medical management option is also preferred for who?
* Non-invasive stress test – if positive proceed to angiography ± PCI, CABG * Also preferred for patients with serious comorbidities or contraindications to PCI
57
NSTE-ACS: Intermediate to high-risk patients * What type of patient usually has PCI within 24 hours?
Superior for patients * > 70 years * Previous MI or revascularization * ST-segment changes * Heart failure * Elevated troponin * Diabetes mellitus * Positive non-invasive stress test
58
Who else it is recommended for to have PCI within 24 hours?
* Refractory angina * Acute heart failure * Cardiogenic shock * Arrythmias
59
NSTE-ACSIntermediate to high-risk patients * What is initiated? * What is preferred for patients with early PCI? Why? * What are the CI?
* Prasugrel or ticagrelor preferred for patients with early PCI * Reduction in cardiovascular death, MI, or stroke compared to clopidogrel * Prasugrel with increased bleeding risk compared to ticagrelor * CI: stroke or TIA
60
NSTE-ACS: Intermediate to high-risk patients * Prasugrel and ticagrelor not recommended for use with what? * Many patients de-escalated to what prior or shortly after hospital discharge? Why?
* Prasugrel and ticagrelor not recommended for use with fibrinolytic therapy (aka – tPA) * Many patients de-escalated to clopidogrel prior to or shortly after hospital discharge due to changes in bleeding risk or cost
61
NSTE-ACS: Intermediate to high-risk patients * What do you need to initate besides P2Y12 inhibitor * What needs to happen with 24 hours?
* Initiate anticoagulation – enoxaparin or unfractionated heparin * Coronary angiography within 24 hours
62
Initial txt of stemi * What is first? * What do you need to immediately do? What is the time goals? (2)
* Initial supportive care=MONA * Immediate reperfusion – angiography / PCI * Goal reperfusion time = ≤90 minutes from arrival in PCI- capable hospital * 120 minutes if emergent transfer required
63
Inital txt of STEMI * What do you need to start after MONA? * When do you give fibroinolysis?
* Initiate P2Y12 inhibitor - any with PCI or clopidogrel with fibrinolysis * Initiate anticoagulation - heparin, LMWH, or bivalirudin * Fibrinolysis: Only when expected time to PCI is > 120 minutes
64
What are the examples of fibrinolytics? * What is the source? * What is the MOA?
65
What are the indications of TPA?
66
What are the absolute contraindications of TPA?
67
What are the absolute contraindications of TPA?
68
# Said FYI but no trust here lol Fibrinolytics:
69
Revascularization: Coronary bypass graft * Useful in those with what? * More efficacious in who? * More beneficial in who?
* Useful in those with left main coronary disease or 3 vessel disease (over 70% stenosis) and LV dysfunction * More efficacious in patients with diabetes * More beneficial in patients with low EF
70
Revascularization: PCI * What med is needed after? How long?
Stent placement standard – needs uninterrupted DAPT for minimum of 1 year
71
Secondary prevention of ischemic event
72
Secondary prevention of ischemic event
73
Secondary prevention of ischemic event
74
summary
75
Cocaine related ACS * Give what? * Do NOT give what?
* Give benzodiazepines as needed for symptom control * Do NOT give beta blockers
76
# ACS * What do you need to stop for all ACS patients? * Correct any what?
* ­Stop NSAID therapy if possible * ­Correct any electrolyte abnormalities, especially hypokalemia and hypomagnesemia, which often occur together.
77
Heart Failure: * Inability of what? * What does the body have to do? * These mechanisms eventually do what?
* Inability of the heart to provide sufficient output to meet metabolic demands of the body * The body has compensatory mechanisms in place to improve CO (makes everything worse) * These mechanisms eventually exacerbate the underlying cardiac problem
78
Heart failure: * Poor cardiac output= _ BP= _ tissue perfusion * What dectects the BP and what does it stimulate?
* Poor cardiac output = decreased BP = decreased tissue perfusion * Baroreceptors in the carotid and aortic sinuses detect low BP and stimulate the sympathetic nervous system ( NE and Epi to stimulate beta receptors -> mroe beta 1)
79
Heart failure: * After NE/Epi is released from sympathetic nervous system, what is stimulated?
Beta and alpha receptors
80
Heart failure: * What happens with beta receptor stimulation?
* Bind to beta-1 cardiac receptors and increase HR and contractility * Bind to beta-1 receptors in kidneys and stimulate JG cells to release renin – RAAS cascade initated (increase BP becasue body is thinking you need more fluid which is not true)
81
Heart failure: * What happens with alpha receptor stimulation?
* Bind to alpha receptors causing vasoconstriction * Increase total peripheral resistance * Venous constriction – increases venous return, preload, stroke volume, CO * Vasoconstriction of afferent arterioles of kidney decreases renal blood flow and stimulate kidneys to retain fluid
82
Heart failure: * What is the new result?
* Heart rate increases – not enough time for bad heart to fill properly * Fluid retention – kidneys (various mechanisms) * Arterial constriction increases afterload * Venous constriction increases preload | Heart struggles
83
Heart failure * most txt is aimed to do what?
Most treatments aim to shut down compensatory mechanisms
84
Heart Failure: HFrEF (systolic HF) * What type of problem? * What diseases? * Reduced what? * Rhythm? * EF?
85
HFpEF (diastolic HF) * What type of problem? * Not enough what? * What are the causes? * What is the EF?
86
What are the sxs of left vs right sided HF?
Left-Pulmonary Right- systemic
87
88
89
HF-treatment goals? (4)?
* Slow and reverse LV remodeling * Reduce symptoms * Improve quality of life * Reduce morbidity and mortality
90
HF txt: * Which drug classes are symtom relief only?
Diuretics, nitrates, digoxin symptom relief only
91
HF: Which drugs deal with long-term management and to improve survival (decrease mortality)?
* ACEI / ARBs * Beta blockers * Aldosterone antagonists * Angiotensin receptor/neprilysin inhibitors * Sodium-glucose co-transporter 2 inhibitors
92
Pharm general prinicipals: * Medications can be started how? What is usually started first then two weeks after? * How do you start the classes of medications?
93
What are the titration intervals for ACE/ARBS? ARNI/BB?hydralazine+nitrates?
* ACE/ARBS – double dose every 1-2 weeks * ARNI/beta blockers/hydralazine + nitrates – double every 2 to 4 weeks
94
What is Stage A and B of HF?
95
What is stage C and D of HF?
96
Stage A- Primary Prevention * What needs to change in life? * Stop what? * What needs to get under control?
* Lifestyle modifications: Physical activity, healthy diet, weight management * Smoking cessation * Hypertension – guideline directed BP control
97
Stage A: Primary prevention * What do you start with a patient with Type 2 DM and CVD or high ASCVD? What does it prevent? * What else to you give for CDV?
98
Stage B: Prevent symtomatic HF * What do you need to start with LVEF <40%? * What do you start with patients with recent MI or ACS?
99
What do you need to avoid in a patient with LVEF <50%? Why? (2)
* Thiazolidinedione hypoglycemics (rosiglitazone, pioglitazone) * Non-dihydropyridine CCB – negative inotropic effects
100
101
Stage C-Symptomatic HF: supportive measures * What type of txt? * Follow what? * What do you need to address?
* Multidisciplinary treatment * Follow guideline directed medical therapy (GDMT) * Address barriers to self care * Reduce hospitalizations * Improve survival
102
Stage C-Symptomatic HF: supportive measures * What do you need to give against resp illness? * Screen for what? * What about diet? * What about movement?
* Vaccination against respiratory illnesses * Screen for depression, social isolation, frailty, low health literacy * Sodium restriction (<2300 g/day); low level evidence * Exercise / cardiac rehabilitation - supervised
103
STAGE C – HFrEF ARNI, ACEI, ARBS: NYHA class II to IV HF * Reduce what? * Lower rates? * Lower incidence of what?
* Reduce total mortality * Lower hospitalization rates * Lower incidence of MI or stroke
104
Stage C– Hfref ARNI, ACEI, ARBs * NYHA class II to III - What is recommended first line? Why? * What is second and third line?
105
* What are Natriuretic peptides and their effects?
Natriuretic peptides – endogenous vasoactive peptides that **reverse effects of angiotensin II (ATII)** * Promote fluid loss, vasodilation * Decreased blood pressure * Decreased cardiac hypertrophy
106
Neprilysin inhibitors: * What does Neprilysin usually do? * what happens if blocked? * What must the drug be given with?
Natriuretic peptides and ATII naturally broken down by neprilysin * Neprilysin inhibition prevents the breakdown of natriuretic peptides * Neprilysin inhibition prevents the breakdown of ATII Must be given with ARB to counteract the effects of increased ATII
107
Sacubitral/Valsartan (entresto) * What are the adverse effects? * What are the CI?
108
Sacubitral/Valsartan (entresto) * What do you need to monitor? * What does the drug increases?
109
Sacubitril / valsartan (entresto):PARADIGM HF trial * What were the primary outcomes?
Primary outcomes – cardiovascular death and hospitalizations rates ## Footnote * 21% of patients taking Entresto vs 26.5% of patient taking enalapril met primary outcomes (p<0.001) * Study stopped earlyðrules of benefit met
110
Stage C-HFrEF BB * Reduces, improves what? * What are the specific agents shown to reduce mortality and hospitalizations?
111
Stage C – HFrEF Beta-blockers * What is the goal?
Goal = reach dose showing benefit in clinical trials * Benefits seen across all patient populations * Benefits are not a class effect
112
Stage C-HFrEF MRAs * What are the examples? * What classes and what does it reduce?
113
Stage C-HFrEF MRAs * What should the patients have? (2) * What do you need monitor closely?
114
Stage C HFrEF SGLT2i * Recommended to who? * Independent of what?
* SGLT2i recommended to reduce HF hospitalization and cardiovascular mortality in patients **with or without type 2 DM** (SYMPTOMS) * Independent of glucose lowering effects
115
Stage C HFrEF SGLT2i * What do the two trails look at? What are the results (3)
Two trials DAPA-F (dapagliflozin) and EMPEROR-REDUCED (empagliflozin) * Patients had a LVEF ≤ 40 %, stage II-IV NYHA HF, and elevated natriuretic peptides Results: * 25% composite reduction in cardiovascular death or hospitalization * Reduction in all cause mortality * Slower decline in eGFR
116
116
Sodium-glucose co-transport 2 inhibitors
117
Sodium-glucose co-transport 2 inhibitors * Effectiveness decreases with what? * Specific agents shown to decrease what?
* Effectiveness decreases with reduction in renal function * Specific agents shown to decrease atherosclerotic CV morbidity and mortality
118
Diuretics: * What does it do? * What is first line? Adjust dose to what? Reponse decrease by what?
Relief of fluid retention to improve symptoms Loop diuretics = first line * Adjust dose to euvolemia; weight loss 0.5 to 1 kg/day * Response decreased by high sodium intake, NSAID use and renal impairment
119
Diuretics: Thiazide Diuretics * Recommended as what? * Patients not responding to what? * Decreases what? * Dual therapy does what?
120
Stage C: HFrEF (hydralazine and nitrates) * Reduces what?
Relief of fluid retention to improve symptoms
121
Stage C- HFrEF: Hydralazine and nitrates * Who is it recommended for? * What does it improve?
122
# She siad FYI Aditional therapies * What does it not do? * May decrease what? * What are the examples (4)
123
Hfref – drugs without benefit / potential harm * Which drug has no benefit?
Dihydropyridine CCBs
124
Hfref – drugs without benefit / potential harm * Which drugs cuase harm and why?
* Nondihydropyridine CCB * IC antiarrhythmics and dronedarone – increased mortality * Thiazolidinediones – worsen symptoms and increase hospitalizations * DPP-4 inhibitors (gliptins) – increase HF hospitalizations * NSAIDS (increase sodium and BP)
125
HFpEF (LVEF >50%) * Therapy similar to what? * What do you need to identify and treat?
Therapy similar to HFrEF – mostly symptomatic benefit Identify and treat underlying causes * Hypertension * Amyloidosis / sarcoidosis * CAD * Atrial fibrillation
126
HFpEF (LVEF >50%) * Diuretic? * What agents decrease hospitalization? * What offer no benefit?
Diuretic therapy as per HFrEF (LOOP) Agents decreasing hospitalization * SGLT2i * Mineralocorticoid receptor antagonists * ARB or ARNI Nitrates offer no benefit
127
What are the four cardiomyopathies?
128
Dilated CMP * What are the causes?
(most common – 95%) * Idiopathic / ETOH (first line-stop alc) * Systolic dysfunction * Low EF * MC in men
129
What are the causes of hypertrophic and restrictive cardiomyopathy?
Hypertrophic Cardiomyopathy * Genetic * Diastolic dysfunction Restrictive Cardiomyopathy * Idiopathic * Systolic & diastolic dysfunction
130
Dilated CMP txt * What do you need to stop? * Treat underlaying what? * **MCC of what?**
* Stop offending agent – drugs, **ETOH**, chemotherapy regimens * Treat underlying CAD / ischemia * **MCC of heart transplantation**
131
Dilated CMP txt * What guidelines do you need to follow? * Why anticoagulations? * Low LVEF < 35% and/or arrythmias may need what?
Follow guidelines for HFrEF * Diuretics / sodium restriction / digoxin – symptom control * ACEI, ARB, beta blockers, mineralocorticoid receptor antagonists – decrease mortality * Do ARNi if meet criteria in HF Anticoagulation for known atrial fibrillation, artificial valve, thrombus Low LVEF < 35% and/or arrythmias may need assist devices / defibrillators
132
Hypertrophic CM * What is the organization of heart? * What are the causes? * Often what?
133
Hypertrophic CM Txt * Avoid what? * Screen who?
* Avoid strenuous exercise or competitive sports * Screen family members
134
Hypertrophic CM * How do you avoid preload reduction (increase preload)? * How do you avoid afterload reduction (increase afterload)?
Avoid preload reduction – increases EDV and decreases outflow obstruction * Adequate hydration * Avoid diuretics * Avoid venodilators – ACEI/ARBs/nitrates Avoid afterload reduction – increases EDV and decreases outflow obstruction * Avoid ACEI/ARBs/hydralazine/dihydropyridine CCB
135
Hypertrophic CM txt * Avoid increasing what? * What is first line? * What is second line? * What do patients need to AVOID?
136
Hypertrophic CM txt: * How do you avoid fatal arrythmias? * Why anticoags? * What are some invasice procedures options?
137
Restrictive cmp: * What happens to heart? * What are the primary and secondary causes?
138
Restrictive CMP txt * Treat what? * What is the main stay txt? * What nnes to be restricted? * What is not generally beneficial * What as needed (3) * What type of transplat? * What is poor?

Pharm II (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions